| Project/Area Number |
17K15093
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Functional biochemistry
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| Research Institution | Osaka Prefecture University |
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Principal Investigator |
Takenaka Nobuyuki 大阪府立大学, 理学(系)研究科(研究院), 准教授 (20610504)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 糖尿病 / Rac1 / インスリン / 脂肪細胞 / 糖取込み / 肥満 / 細胞内シグナル伝達 / 糖取り込み / GLUT4 / 白色脂肪細胞 / 脂肪酸取り込み / 低分子量GTP結合タンパク質 / シグナル伝達 / 細胞・組織 |
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| Outline of Final Research Achievements |
Insulin stimulates glucose uptake in skeletal muscle and adipose tissue, thereby regulating the blood glucose level. In this study, we aimed to clarify the role and regulatory mechanisms of small GTPase Rac1 in adipocyte insulin signaling by using in vitro-differentiated 3T3-L1 adipocytes and mouse models. We identified a novel signaling mechanism whereby the guanine nucleotide exchange factor FLJ00068 activates Rac1 downstream of the protein kinase Akt2. Moreover, we identified the RalA regulates glucose uptake downstream of Rac1 in adipocytes.
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| Academic Significance and Societal Importance of the Research Achievements |
糖尿病の発症原因の1つに脂肪細胞でのインスリン応答性糖取込み機構の異常が示唆されているが、不明な点が多い。今回の研究により明らかになったRac1を介した新たな糖取込み機構は、糖尿病に対する新たな治療法の創出につながると考えられる。
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